ELECTROPHYSIOLOGY
Drug-induced pericarditis mimicking Brugada syndrome
Cardiology Department, Amiens-Picardie University Hospital, Service de Cardiologie A, Groupe Hospitalier Sud, Avenue René Laënnec, 80054 Amiens Cedex 1, France
Manuscript submitted 29 June 2006. Accepted after revision 27 September 2006.
* Corresponding author. Tel: +33 3 22 45 58 75; fax: +33 3 22 45 56 61. E-mail address: hermida.jean-sylvain{at}chu-amiens.fr
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Abstract |
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Brugada syndrome (BS) is associated with sudden cardiac death in patients with a structurally normal heart. The ECG pattern of BS has also been described in patients with myocardial abnormalities. Cardiac hypersensitivity and myopericarditis have been reported during long-term treatment with mesalazine. We report the case of a man, treated with mesalazine for Crohn's disease who developed drug-induced pericarditis. The ECG showed a coved ST-segment elevation in the right precordial leads V1–V3, a pattern mimicking BS. The ECG normalized in a few days after mesalazine withdrawal and the follow-up was uneventful. The ECG remained normal. Two ajmaline tests were both negative and ruled out the diagnosis of BS. This observation illustrates that a coved ST-segment elevation in the right precordial leads should not be, systematically, regarded as a marker of a specific syndrome, but may also reflect a common electrical manifestation of abnormalities in the right ventricle or pericardium.
Key Words: Brugada syndrome, Mesalazine, ST-segment elevation, Pericarditis
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Introduction |
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Cardiac hypersensitivity to mesalazine was reported in the late 1980s.1
Shortly after, Kristensen et al.2 showed that mesalazine could be associated with ventricular fibrillation and fatal myocarditis. The period between the onset of treatment and the appearance of the cardiac signs ranged from a few days to 6 years and the mechanism of mesalazine-induced myopericarditis might have an allergic origin. Brugada syndrome (BS) is a channelopathy characterized by episodes of syncope, ventricular fibrillation, or sudden cardiac death in patients with structurally normal hearts. It is characterized by ST-segment elevation in the right precordial electrocardiographic (ECG) leads spontaneously or after ajmaline or flecainide administration. The BS is conventionally thought of as a primary electrical heart disease arising in a myocardium that is otherwise structurally and functionally normal. Nevertheless, it is becoming increasingly recognized that some types of myocardial pathology occur in patients with the clinical picture of BS. |
Case report |
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A 44-year-old man was admitted with sudden severe chest pain. For the previous 4 years, he had been successfully treated with mesalazine 3 g daily for Crohn's disease. Until the day of admission, he was free of any intestinal or extra-intestinal manifestation of his inflammatory bowel disease, as well as from any side-effect of therapy. The chest pain was not aggravated by lying in the supine position and was relieved by sitting up and leaning forward. There was neither any sign of heart failure nor precordial friction rub and the physical examination was unremarkable.
On admission, laboratory tests yielded the following results: white blood cell count, 10.7 x 109/L with 4.7% eosinophils; erythrocyte sedimentation rate, 42 mm/h (2 < N < 10 mm/h); C-reactive protein, 13.7 mg/L (N < 5 mg/L); troponin I, 0 µg/mL (N < 1.5 µg/mL); myoglobin, 62.4 µg/L (N < 90 µg/L); creatine kinase, 99 U/L (N < 239 U/L); urea, 16.3 mmol/L (2.5–6.7 mmol/L); alkaline phosphatase, 305 UI/L (N < 270 UI/L); and creatinine, 305 µmol/L (N < 115 µmol/L). Chest radiography revealed normal findings and echocardiography showed normal left ventricular function with no pericardial effusion. The initial ECG showed a coved ST-segment elevation in the right precordial leads V1–V3 and a pattern mimicking a coved-type BS (Figure 1A). Normal heart enzyme and troponin levels argued against myocarditis. A few days after stopping the mesalazine medication, the chest pain disappeared and ECG normalized. An ajmaline test was carried out and was negative. The patient was not inducible during programmed ventricular stimulation. A diagnosis of pericarditis was retained for this patient on the basis of the clinical feature of the pain, the lack of variation of the cardiac enzymes, and the ST-segment elevation. The patient was discharged home with corticosteroid treatment for concomitant interstitial nephritis, which had been diagnosed by kidney biopsy.
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Six months later, the patient remained well and symptom-free and his ECG was normal (Figure 1B). A repeat ajmaline test was negative, ruling out the diagnosis of BS.
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Discussion |
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A wide range of conditions may lead to a Brugada-type ECG: fever, right ventricular pathology, electrolyte abnormalities, and pharmacological sodium channel antagonism. Different groups of drugs, with a sodium channel antagonism effect, may induce the ECG Brugada sign: class IA antiarrhythmic drugs, class IC antiarrhythmic drugs, cocaine, tricyclic antidepressants, and dimenhydrinate. In these different conditions, the Brugada ECG pattern disappears within a few days of withdrawal. The ECG pattern of BS can account for two mechanisms: (i) conduction delay in the outflow tract of the right ventricular epicardial free wall or (ii) premature repolarization of the right ventricular epicardium secondary to loss of the action potential dome.3
Our study illustrates the development of Brugada signs in a case of mesalazine-induced pericarditis. The possibility of an unmasking ST-segment elevation in an asymptomatic BS, previously reported,4 has been excluded. Few studies have highlighted the complexities between the ECG manifestations of BS and the presence of structural heart disease. The observations reported by Frustaci et al.5 demonstrated that some patients who present with clinical manifestations of BS may have structural heart disease which contributes to the expression of the clinical syndrome. The prevalence of latent forms of BS reaches 0.5% in the healthy population.6 It seems likely that some of these patients may have primary heart muscle disease.
These observations provide further evidence that pericarditis may mimic BS and may account for the transient development of the characteristic ECG abnormalities in some patients. In some cases, the ECG pattern of ST-segment elevation in the right precordial leads should not be regarded as a marker of a specific syndrome, but rather a common electrical manifestation of abnormalities in the right ventricle or pericardium.
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References |
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[1] Agnholt J, Sorensen HT, Rasmussen SN, et al. Cardiac hypersensitivity to 5-aminosalicylic acid. Lancet 1989; 1: 1135.[Web of Science][Medline]
[2] Kristensen KS, Hoegholm A, Bohr L, et al. Fatal myocarditis associated with mesalazine. Lancet 1990; 335: 605.[Web of Science][Medline]
[3] Yan GX and Antzelevitch C. Cellular basis for the Brugada syndrome and other mechanisms of arrhythmogenesis associated with ST-segment elevation. Circulation 1999; 100: 1660–66.
[4] Kurisu S, Inoue I, Kawagoe T, et al. Acute pericarditis unmasks ST-segment elevation in asymptomatic Brugada syndrome. Pacing Clin Electrophysiol 2006; 29: 201–3.[CrossRef][Medline]
[5] Frustaci A, Priori SG, Pieroni M, et al. Cardiac histological substrate in patients with clinical phenotype of Brugada syndrome. Circulation 2005; 112: 3680–7.
[6] Hermida JS, Jandaud S, Lemoine JL, et al. Prevalence of drug-induced electrocardiographic pattern of the Brugada syndrome in a healthy population. Am J Cardiol 2004; 94: 230–3.[CrossRef][Web of Science][Medline]
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